Hippocampal β2‑microglobulin mediates sepsis‑induced cognitive impairment
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Abstract:
Acute brain dysfunction is a frequent complication in sepsis patients and is associated with long‑term neurocognitive consequences and increased mortality, yet the underlying mechanism remains unclear. Emerging evidence has suggested that β2‑microglobulin [a component of major histocompatibility complex (MHC) class I molecules] is involved in cognitive dysfunction in various neurological diseases. Therefore, the present study tested the hypothesis that β2‑microglobulin in the brain also mediates sepsis‑induced cognitive impairment. In the present study, wild‑type and antigen processing 1 (Tap1)‑deficient mice (Tap1‑/‑) were subjected to cecal ligation and puncture (CLP). Survival rate, cognitive function, and biochemical analysis were performed at the indicated time points. The data revealed that CLP induced anxiety‑like behavior and impaired hippocampal‑dependent contextual memory in wild‑type mice, which was accompanied by hippocampal microglial activation, increased level of interleukin‑1β, and decreased concentrations of brain derived neurotrophic factor and postsynaptic density protein 95. Notably, it was demonstrated that Tap1‑/‑ mice with reduced cell surface expression of MHC I protected mice from anxiety‑like behavior and impaired hippocampal‑dependent contextual memory and reversed most of these biochemical parameters following sepsis development. In summary, the results of the present study suggest that β2‑microglobulin negatively regulates cognitive impairment in an animal model of sepsis induced by CLP.Keywords:
Neurocognitive
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Ojbective To study the difference of Aβ 25-35 on neurons between hippocampus and septum. Mdthods employing the method of primary cell culture, neurons survival and SOD were examined ,and amalysed the expression of apoptosis-related gene bcl-xl by Western blot. Result Aβ 25-35 might reduce the survival of hippocampal and septal neurons, increased both activity of CuZn-SOD and expression of Bcl-xl, but decreased the activity of Mn-SOD of hippocampal neurons, and had on obvious effect on septal neurons. Conclusion Aβ 25-35 had the same effect on survival and CuZn-SOD but Mn-SOD between the hippocampus and septum. The cytoxic mechanisms of Aβ 25-35 on hippocampus and septus might be different.
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Neocortex
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The mammalian hippocampal formation (HF) is organized into domains associated with different functions. These differences are driven in part by the pattern of input along the hippocampal long axis, such as visual input to the septal hippocampus and amygdalar input to the temporal hippocampus. HF is also organized along the transverse axis, with different patterns of neural activity in the hippocampus and the entorhinal cortex. In some birds, a similar organization has been observed along both of these axes. However, it is not known what role inputs play in this organization. We used retrograde tracing to map inputs into HF of a food-caching bird, the black-capped chickadee. We first compared two locations along the transverse axis: the hippocampus and the dorsolateral hippocampal area (DL), which is analogous to the entorhinal cortex. We found that pallial regions predominantly targeted DL, while some subcortical regions like the lateral hypothalamus (LHy) preferentially targeted the hippocampus. We then examined the hippocampal long axis and found that almost all inputs were topographic along this direction. For example, the anterior hippocampus was preferentially innervated by thalamic regions, while the posterior hippocampus received more amygdalar input. Some of the topographies we found bear a resemblance to those described in the mammalian brain, revealing a remarkable anatomical similarity of phylogenetically distant animals. More generally, our work establishes the pattern of inputs to HF in chickadees. Some of these patterns may be unique to chickadees, laying the groundwork for studying the anatomical basis of these birds' exceptional hippocampal memory.
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Using quantitative receptor autoradiography, spirodecanone binding was evaluated in the gerbil hippocampus 1 h-1 month after cerebral ischaemia of 10 min. The spirodecanone binding was unaffected in the hippocampus up to 48 h after ischaemia. Thereafter, increased binding was found in the stratum radiatum of hippocampal CA1 sector 7 days and 1 month after ischaemia. Other hippocampal regions showed no significant alterations in the spirodecanone binding. A histological study revealed that the hippocampal CA1 sector was severely damaged 7 days and 1 months after ischaemia. These results demonstrate that spirodecanone binding sites are located on interneurones or glial cells in the hippocampal CA1 sector.
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Individuals at clinical high risk for psychosis (CHR) exhibit neurocognitive deficits in multiple domains. The aim of this study is to investigate whether several components of neurocognition are predictive of conversion to psychosis.Fifty-two CHR individuals were assessed with the Structured Interview for Psychosis Risk Syndromes and completed a battery of neurocognitive tests at baseline including measures of executive functioning, attention, working memory, processing speed and reaction time. Neurocognitive functioning at baseline was scored based on an external normative control group. Most subjects were followed for 2.5 years to determine conversion status.Significant differences in neurocognitive functioning between CHR individuals and the control group were present in all domains. Twenty-six per cent of the participants converted to psychosis within 9.8 (standard deviation = 8.0) months on average (median 9 months), but there were no significant differences in neurocognition converters and non-converters.Individuals at CHR have deficits in neurocognitive functioning, but such deficits do not appear to be related to conversion risk.
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HIV infection is associated with disturbances in brain function which reflect themselves in HIV associated neurocognitive disorder (HAND). Neurocognitive examination is a sensitive and relevant approach to detecting and monitoring HAND. The approaches to evaluating the various neurocognitive disturbances are reviewed, along with consideration of cofactors that may influence expression of these disorders.
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In this study, I investigate the role that hippocampal inhibitory cells (intemeurons) have on the synchronization of oscillations between the two hemispheres of the hippocampus. My study focuses in particular on the ripple oscillations, because this network activity is highly synchronous between left and right hippocampus. My hypothesis is that a subset of hippocampal intemeurons might establish axonal connections from the hippocampal area in which the somata reside towards the contralateral side, hence regulating inter-hippocampal ripple discharges. I address this hypothesis injecting in one side of the hippocampus substance P fragment, a peptide that increases the activity of subsets of inhibitory neurons in rat hippocampus, and the antimalarial Quinine whose roles as gap-junction blocker has been well established by numerous publications. Simultaneous recording from both hippocampi are thus compared to investigate whether ipsilateral injected drugs affect hippocampal ripple activity recorded contralaterally. I found that ripple oscillations are indeed affected by injection of the abovementioned drugs: Quinine increases length and decreases Inter Ripple Interval (I.R.I.) in both injected and contralateral hippocampus; on the other hand, SP decreases the average amplitude of the ripple episode, but increases the duration of the ripple event. Most importantly, many of the perturbations observed were preserved between injected and contralateral hippocampus. Since the drugs I employed affect mainly inhibitory neurons, I propose that long-range projecting inhibitory neurons located in the injected hippocampus are responsible for carrying the drugs' effects to the contralateral hippocampus. In conclusion, my results seem to indicate that long-range projecting intemeurons are involved in transmitting ripple synchronization information across the two hippocampi.
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